The epileptic state is probably initiated by small, subtle changes in the membrane characteristics of neurons within the involved region of the brain. These small alterations are then amplified by the recurrent positive feedback system, resulting in the seizure. It is difficult, if not impossible to locate and define these small changes in membrane activity in the mammalian cortex due to the great architectonic and functional complexity of the tissue. This study will therefore use less complex, isolated neuronal preparations; the crayfish stretch receptor cell and cells of the abdominal ganglion of Aplysia. In part, this investigation will attempt to clarify the electrochemical mechanisms underlying the alterations in function of these neuronal elements, induced by treatment with certain convulsant and anticonvulsant drugs. These mechanisms will be explored through a study of basic membrane properties such as: 1) membrane conductance and the specific ions involved; 2) active transport; 3) synaptic transmission; 4) membrane potential stability; and 5) paroxysmal-like activity--using synaptic voltage clamping, ion-specific microelectrodes and other standard electrophysiological techniques. Our study will also include an investigation of the convulsant and anticonvulsant drug-induced modification of the known, integrated electrophysiological activity of a well-identified, interacting, neuronal population found in the abdominal ganglion of Aplysia. We have, therefore, substituted well-defined, isolated neuronal elements and populations for the complex mammalian cortex in an attempt to delineate the mechanism responsible for seizure initiation and termination.